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Chronic myelogenous leukemia (CML) is characterized by the _expression_ of
the BCR-ABL tyrosine kinase, which results in increased cell proliferation and
inhibition of apoptosis. In this study, we show in both BCR-ABL cells (Mo7e-p210
and BaF/3-p210) and primary CML CD34+ cells that STI571 inhibition of BCR-ABL
tyrosine kinase activity results in a G(1) cell cycle arrest mediated by the
PI3K pathway.
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